钾-氯离子协同转运体2信号通路与神经病理性疼痛的关系

The relationship between KCC2 signaling pathway and neuropathic pain

神经病理性疼痛(Neuropathic pain,NP)由神经炎症所诱发,主要表现为慢性疼痛和疼痛感觉异常等,常引发焦虑、抑郁和社交障碍,发病率也呈逐年上升态势。神经病理性疼痛发病机制复杂,其中钾-氯离子协同转运体2(K+-Cl-cotransporter 2,KCC2)是调节神经病理性疼痛的重要信号分子,也是神经病理性疼痛的治疗靶点。同时,神经病理性疼痛的干预手段也较局限,而运用电针治疗由选择性坐骨神经分支损伤(Spared nerve injury,SNI)诱导的神经病理性疼痛已得到广泛认可,但其具体作用的分子路径尚不明确。本文对KCC2信号通路与神经病理性疼痛的关系进行综述,为进一步探讨KCC2信号通路是否可能参与电针治疗神经病理性疼痛的过程提供理论依据。

Neuropathic pain(NP)is induced by neuroinflammation,which is characterized by chronic pain and abnormal sensation of pain,and often causes anxiety,depression and impaired social interaction.The pathogenesis of neuropathic pain is complex.KCC2 signal molecule is an important pathway regulating neuropathic pain,and is also a therapeutic target of neuropathic pain.The use of electroacupuncture(EA)in the treatment of neuropathic pain induced by spared nerve injury(SNI)has been widely recognized.But the specific molecular pathway of its action is not yet clear.This article reviews the relationship between KCC2 signaling pathway and neuropathic pain in order to provide a theoretical basis for further analysis of the possible therapeutic approaches to neuropathic pain.